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Videos de Conceptos Relacionados

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
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Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

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Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
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Drugs for Treatment of Crohn's Disease in IBD Using Immunomodulatory Agents01:29

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Crohn's disease is an inflammatory bowel disorder marked by chronic inflammation of the GI tract. Various treatment strategies for Crohn's disease are employed, such as immunomodulatory agents, glucocorticoids, and biologics or anti-TNF therapy. Azathioprine (Imuran), a commonly used immunomodulatory drug for Crohn's disease, is converted in the body to mercaptopurine, which inhibits purine biosynthesis and cell proliferation. Both are utilized in severe cases of Inflammatory Bowel...
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Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

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Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...
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Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

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Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
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Video Experimental Relacionado

Updated: Sep 9, 2025

A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis
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A Modified Two Kidney One Clip Mouse Model of Renin Regulation in Renal Artery Stenosis

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La ciclooxigenasa-2 de los fibroblastos asociada a los riñones restringe las metillargininas y la trombosis:

Maria E Lopes-Pires1, Fisnik Shala1, Ugo Soffientini1

  • 1National Heart & Lung Institute, Imperial College London, London, UK.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology
|August 28, 2025
PubMed
Resumen

Los antiinflamatorios no esteroideos (AINE) aumentan el riesgo trombótico al inhibir la ciclooxigenasa-2. La deficiencia de ciclooxigenasa-2 en los fibroblastos exacerba este riesgo a través de la desregulación de la metilarginina, destacando su papel en la protección cardiovascular.

Palabras clave:
Dimetilaginina asimétrica y sus derivadosel endotelioel riñónlas metillargininasÓxido nítricomedicamentos antiinflamatorios no esteroideosProstaciclina y sus derivadosTrombosis

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Área de la Ciencia:

  • Ciencias cardiovasculares
  • Fisiología renal
  • Farmacología

Sus antecedentes:

  • Los antiinflamatorios no esteroideos (AINE) inhiben la ciclooxigenasa-2 (COX-2) y están relacionados con un aumento de los eventos cardiovasculares trombóticos.
  • La actividad renal de la COX-2 está implicada en los efectos secundarios cardiovasculares inducidos por los AINE, potencialmente a través de las vías de la metilarginina.
  • La falta de modelos específicos ha dificultado la comprensión del papel de la COX-2 renal.

Objetivo del estudio:

  • Investigar las contribuciones específicas de la ciclooxigenasa-2 (COX-2) en diferentes tipos de células a los riesgos cardiovasculares asociados a los AINE.
  • Aclarar los mecanismos subyacentes a los efectos pro-trombóticos observados con el uso de AINE.

Principales métodos:

  • Modelos de ratón generados y analizados con deleción dirigida de la ciclooxigenasa-2 (COX-2) en fibroblastos y células endoteliales.
  • Evaluar la trombosis después de la lesión arterial, los niveles plasmáticos de metilarginina y la función de la óxido nítrico sintasa (NOS).
  • Se evaluaron los efectos de la administración de L-arginina en los fenotipos pro-trombóticos.

Principales resultados:

  • La deficiencia de COX-2 en los fibroblastos condujo a un aumento de la trombosis, el aumento de las metilargininas plasmáticas y la disfunción sistémica del óxido nítrico en el endotelio.
  • El fenotipo pro-trombótico en los ratones con KOX-2 de fibroblastos fue revertido por la L-arginina.
  • Los ratones con knockout endotelial de COX-2 exhibieron fenotipos pro-trombóticos a través de un mecanismo vascular, independiente de los cambios en la metilarginina y el tratamiento con L-arginina.

Conclusiones:

  • Los fibroblastos y la ciclooxigenasa-2 renal (COX-2) juegan un papel crucial en la protección antitrombótica.
  • Los efectos secundarios cardiovasculares inducidos por los AINE implican vías influenciadas por la regulación de la COX-2 de los fibroblastos y la metilarginina.
  • La orientación hacia estas vías específicas puede ser esencial para prevenir las complicaciones cardiovasculares relacionadas con los AINE.